We are employing rat liver induced to regenerate by means of partial hepatectomy as a model for studying growth regulation in mammalian cells. Humoral control of liver regeneration is now well established; recent reports stress portal blood hepatotrophic factors. The response to partial hepatectomy in rats eviscerated of portal splanchnic organs, and maintained by continuous intravenous infusion, affords a new and direct means of evaluating such factors, since only in such animals can insulin, glucagon, and various substrates and metabolites normally derived from intestinal absorption be examined independently. Regenerative activity (DNA synthesis) is delayed and reduced in magnitude, but unequivocally present, at least during the first several days after evisceration. Insulin augments the response; whether or not it can serve as a primary initiator is now being investigated. Its action will also be studied in conjunction with glucagon, added substrates, metabolites, and other hormones, which will in turn be studied individually and in combinations. In eviscerated rats we have discovered that the hepatic artery alone suffices to support regeneration; this affords the novel opportunity of administering fractionated blood constituents from normal and partially hepatectomized animals directly into the portal vein remnant. Attempts to clarify the regulatory mechanisms in hepatic regeneration involve also a quest for the growth related intracellular changes that humoral agents generate. We are currently studying microtubule proteins (tubulins), because of their direct participation in the events of mitosis, and because of their possible role in mitogenesis. (Little is known about tubulins in mammalian organs other than brain.) Liver homogenates contain soluble and particulate tubulin fractions; the amount and rate of synthesis of soluble tubulins increases coincident with DNA synthesis and mitosis. Particulate tubulins require further study. A major extension of this work will include detailed investigation of tubulins derived from hepatomas, and a variety of neoplastic and transformed cells, an area hitherto largely unexplored, but possibly fruitful because of the prevalence of mitotic abnormalities in neoplastic tissues.